Congestive cardiac failure

Chaze Kamuwanga
 Definition
Congestive cardiac failure (heart
failure) is the inability of the heart to
supply sufficient blood flow to meet
the body needs
 Classification
There are many different ways to
categorise heart failure including:
1. whether the abnormality is due to
insufficient contraction and/or
relaxation of the heart that is systolic
dysfunction versus diastolic
dysfunction
 Classification
2. the side of heart involved that is
left heart failure (LHF) versus right
heart failure (RHF). LHF
compromises aortic flow to the body
and brain. RHF compromise
pulmonic flow to the lungs. Mixed
presentation occurs when cardiac
septum is involved
 Pathophysiology
Heart failure is caused by any
condition which reduces the
efficiency of the myocardium or
heart muscle, through damage or
over loading. Hence there are diverse
conditions that may cause it e.g.
myocardia infarction, hypertension
 Pathophysiology
The over load or increase in
workload eventually produces the
following compensatory changes on
the heart that may enable the
weakened heart to continue to meet
the metabolic demands of the body:
 Pathophysiology
According to Frank Starling law of
the health heart which states that
within limits, cardiac muscle fibers
contract more forcibly the more they
are stretched before a contraction.
 Pathophysiology
By increasing venous return to the
heart, the fibers are stretched, which
allows for a more forceful
contraction thus increasing the stroke
volume and resulting in increased
cardiac output.
 Pathophysiology
However, the mechanism of
ventricular dilatation fails in heart
failure as there is reduced force of
contraction and a reduced stroke
volume.
Reduced force of contraction is due
to over loading of the ventricle
 Pathophysiology
The ventricle is loaded with blood to
the point where muscle contraction
becomes less efficient.
This is due to reduced ability to cross
link actin and myosin filaments in
over stretched heart muscle.
 Pathophysiology
Stroke volume is reduced due to a
failure of systole, diastole or both.
Increased end systolic volume is
usually caused by reduced
contractility. Decreased end diastolic
volume results from impaired
ventricular filling (when compliance
falls i.e. walls stiffen).
 Pathophysiology
Tachycardia: stimulated by increased
sympathetic activity to maintain
cardiac output to compensate for
heart failure by maintaining blood
pressure and perfusion. This places
further strain on the myocardium to
increase coronary perfusion
requirements
 Pathophysiology
However, as the heart rate continues
to increase diastole is shortened to
the point where an inadequate filling
of the ventricles occurs and cardiac
output actually decreases. As a result
ischaemic heart disease worsens or a
fatal arrhythmia may occur
 Pathophysiology
Hypertrophy of the myocardium: an
increase in the diameter of muscle
fibers is seen as thickening in the
walls of the heart. This increase in
the muscle mass results in more
effective contraction of the heart
further increasing cardiac out put
 Pathophysiology
However this compensatory
limitation has a limitation as muscle
mass out grows the coronary artery
supply resulting in hypoxia and
decreased effectiveness. It may also
contribute to the increased stiffness
and decreased ability to relax during
systole
 Pathophysiology
There is enlargement of the ventricles
contributing to the enlargement and
spherical shape of the failing heart.
The increase in ventricular volume
also causes a reduction in stroke
volume due to mechanical and
contractile inefficiency
 Pathophysiology
There is reduced spare capacity: as
the heart works harder to meet
normal metabolic demands, the
amount of cardiac output should
increase in times of increased oxygen
demand (e.g. exercise) but it is
reduced i.e. exercise intolerance
 Pathophysiology
This phenomena signifies the loss of
ones cardiac reserve. Cardiac reserve
is the ability of the heart to work
harder during exercise or strenuous
activity to meet the metabolic
demands.
 Pathophysiology
The general effect of the cardiac
compensatory mechanism is one of
reduced cardiac output and increased
strain on the heart. This increases the
risk of cardiac arrest and reduces
blood supply to the rest of the body.
 Pathophysiology
In chronic disease when cardiac
compensatory mechanisms become
inadequate to continue to meet the
metabolic demands of the body,
homeostatic compensatory
mechanisms are activated some of
which are part of the disease process
 Pathophysiology
Arterial blood pressure falls leading
to vasoconstriction to restore blood
pressure and also increases peripheral
resistance, increasing the workload of
the heart.
 Pathophysiology
As the myocardium increases heart
rate and make more forceful
contractions to increase cardiac
output. Therefore increasing the
amount of work the heart has to
perform.
 Pathophysiology
As the circulating blood volume is
decreased, increased sympathetic
stimulation of hypothalamus (to
secrete vasopressin which causes
fluid retention) and release of
norepinephrine resulting in
generalised vasoconstriction. Hence
increased b/volume and b/pressure
 Causes
Ishaemic heart disease
Cigarret smoking
Hypertension
Obesity
Diabetes
Valvular heart disease
 Rare causes
Viral myocarditis
Infitrations of the muscle such as
amyloidosis
HIV cardiomyopathy
Connective tissue diseases such as
systemic lupus erythematosus
Arrythmias
 Clinical Features
Left Sided Failure: backward failure
of the left ventricle or atrium that
causes congestion of the pulmonary
vasculature leading to the following:
Dyspnea (shortness of breath)
Orthopnea (breathlessness on lying
flat).
 Left sided failure
Paroxysmal nocturnal dyspnea
Easy fatigability
Exercise intolerance
Cardiac asthma (wheezing)
Dizziness
Confusion
Cool extremities at rest
 Right sided failure
Backward failure of the right
ventricle leads to congestion of
systemic capillaries generating
excess fluid accumulation in the body
Peripheral edema or anasarca
Nocturia (frequent nighttime
urination)
 Right sided failure
Ascites (fluid accumulation in the
abdominal cavity causing swelling)
Hepatomegaly (enlargement of liver)
Jaundice (due to liver congestion
leading to impaired liver function)
Coagulopathy (decreased blood
clotting)
 Medical Management
Physical examination: edema found
Echocardiography: to diagnose
cardiac failure and identify valvular
heart disease
Chest Xray: may show cardiomegaly
(visible enlargement of the heart)
 Medical management
Electrocardiogram: to identify right
and left ventricular hypertrophy,
arrhythmias, ischaemic heart disease,
and conduction delay or abnormality
Blood: renal function, liver function
tests, thyroid function tests and full
blood count.
 Diagnosis criteria
Requires Two major or one major
criteria and one minor criteria
Major criteria
Cardiomegaly
Acute pulmonary edema
Paroxysmal
 Major criteria
Crackles on lung auscultation
Jugular vein distension
Weight loss
 Minor criteria
Tachycardia (more than 120/minute)
Nocturnal cough
Dyspnea on ordinary exertion
Pleural effusion
Hepatomegaly
Bilateral ankle edema
 Treatment
ACE inhibitors: enalapril, captopril,
lisinopril, ramipril
Diuretics
Beta blockers
Digoxin (lanoxin)
 Nursing care
Environment: Well ventilated for free
circulation of air
Cool for patients comfort
Well lit for easy observation
Near nurses bay for easy observation
Clean to prevent infection
 Relieve dyspnoae
Administer by nasal cannula at 2-6
litres/minutes
Patient should be well supported in
semi fowlers or high fowlers
position
 Observations
Temperature, pulse, BP checked hourly,
2, 4, 6, 12 hourly to assess for signs of
decreased cardiac output.
Check respirations hourly, 2, 4, 6, 12 to
identify pulmonary congestion and fluid
over load.
Observe patients response to activity
(check P, R and BP during and after an
activity) to monitor condition
 Observations
Strict intake and out put to monitor
renal function and fluid status.
Weekly weight checking to assess for
weight gain
Assess peripheral and sacral oedema
to monitor the condition

 Position
Nurse patient in sitting up position or
elevate the head of the bed to 30 to
45 degrees and provide a padded
cardiac table/pillow on cardiac table
to reduce venous return, reduce
oxygen demand and maximise chest
excursion.
 Position
Accessories like sand bags and
pillows may be used to support the
patient.
 Rest and activity
Encourage rest to conserve energy
Nursing activities in blocks to
promote rest
Measures to maintain a noise free
environment like oiling trolleys
Provide diversional therapy to
conserve energy
 Rest/Activity
Reduce physical activity (offer
bedpan/urinal) to decrease cardiac
workload and reduce oxygen
demands. As patient improves
progressively increase activity to
increase cardiac tolerance.
 Nutrition
Restrict sodium intake: no added salt,
no potato chips
Increased intake od potassium like
banas
Vitamin supplements
 Psychological care
Explain disease process to promote
cooperation
Explain every procedure to promote
cooperation and allay anxiety
Allow patient to ask questions and
answer them truthfully
 Elimination
Avoid straining at defaecation which
places an extra burden on the heart.
During straining against a closed
glottis (Valsavas maneuver), venous
return to the heart is increased as a
result of increased intrathoracic
pressure creating an increased work
load for the heart
 IEC
NUTRITION: Low sodium diet
(avoid table salt, avoid salty foods)
to prevent fluid retention.
Low fat diet for instance milk
without fat, meat without fat, no
fries to prevent excessive weight
gain.
 Nutrition
Fluid intake is restricted to prevent
fluid overload.
High roughage food to prevent
staining at stool.
 Activity
Teach patient how to check pulse rate
to identify excessive cardiac effort.
Instruct the patient to reduce activity if
pulse increases to >20 beats/minute
and to avoid activity if resting pulse is
>100 beats/minute
Advise to avoid strenuous physical
activities.